* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download Ask the Expert: Depression Presenter: Kenneth J. Herrmann, MD
Dissociative identity disorder wikipedia , lookup
Spectrum disorder wikipedia , lookup
Antipsychotic wikipedia , lookup
Generalized anxiety disorder wikipedia , lookup
Abnormal psychology wikipedia , lookup
Schizoaffective disorder wikipedia , lookup
Mental status examination wikipedia , lookup
Critical Psychiatry Network wikipedia , lookup
Emergency psychiatry wikipedia , lookup
Moral treatment wikipedia , lookup
History of psychiatric institutions wikipedia , lookup
History of mental disorders wikipedia , lookup
Pyotr Gannushkin wikipedia , lookup
Bipolar disorder wikipedia , lookup
Child psychopathology wikipedia , lookup
History of psychiatry wikipedia , lookup
Bipolar II disorder wikipedia , lookup
Controversy surrounding psychiatry wikipedia , lookup
Postpartum depression wikipedia , lookup
Behavioral theories of depression wikipedia , lookup
Major depressive disorder wikipedia , lookup
Evolutionary approaches to depression wikipedia , lookup
Biology of depression wikipedia , lookup
Antidepressant wikipedia , lookup
Ask the Expert: Depression Presenter: Kenneth J. Herrmann, MD NAMI Conference Spring 2014 Kenneth J Herrmann M.D. Medical School at Chicago Medical School Internship, residency in general psychiatry, fellowship in child and adolescent psychiatry at the University of Iowa Formerly, Medical Director of Youth Services at the Mental Health Center of Dane Co. Psychiatric Consultant, Psychiatric Services SC, www.psychsvcs.com/ Past Vice-President, Board of Directors NAMI WI Principal, My World Defense, A Healthcare Security Company, http://myworlddefense.com/ Diagnosis of Major Depressive Disorder Irritable/Depressed mood, diminished pleasure/interest Weight changes of greater than 5% in one month Insomnia or hypersomnia Psychomotor agitation or retardation Fatigue or loss of energy, poor concentration Feelings of worthlessness, suicidal thoughts, guilt Etiology of Depression Genetic factors Personality and environmental factors Biochemical abnormalities Prognosis - Adolescence Depression -Duration average of 7 1/2 months -44% in remission within 6 months of Dx -92% recovered by 1 ½ years -72% recurrence within five years EPIDEMIOLOGY Depression: -2% of children in general population -7% depression in children admitted to Hospital -40% children in ped neuro clinics with headaches=depression -4.7% ages 14-16 (3.3% dysthymia) (as age increases female rates increase) -one in five adolescents by age 20 -Lifetime: Males 12% Females 25% Trends for Affective Disorders Age at onset is decreasing Incidence is increasing Risk Factors For Mood Disorders Substance Use Prematurity Family History Head Injury Limitations of Current Research Hard to recruit for certain disorders FDA requirements for drug approval Funding Exclusion criteria Dropout rates Liability Time from idea to publication The Treatment for Adolescents with Depression Study (TADS) Moderate to severe depression Fluoxetine alone or in combo with CBT 13 academic and community sites in the US 12-17 yrs old Combined > mono 42 week total study time Study start 7/98, completed 3/04 Arch. Gen. Psychiatry 10/07 Thinking Outside the Box? FDA warnings and the Antidepressants ? Adequate information ? Diagnosis Increase in antidep. use / decrease in suicides over 10 years prior to warning CONCLUSIONS: In both the United States and the Netherlands, SSRI prescriptions for children and adolescents decreased after U.S. and European regulatory agencies issued warnings about a possible suicide risk with antidepressant use in pediatric patients, and these decreases were associated with increases in suicide rates in children and adolescents. Gibbons etal. Am J. Psychiatry 9/07 Diagnostic Accuracy is Most Important Mania/Bipolar Affective Disorder (BPAD) Elevated, expansive or irritable mood Inflated self-esteem or grandiosity Decreased need for sleep More talkative (distractible) Flight of ideas or racing thoughts Increase in activity Foolish indulgencies Characteristics of BPAD in Children Grandiosity Inappropriate sexual interest Psychotic symptoms “Ultrarapid” cycling Mood Disorder Questionnaire Has there ever been a period of time when you were not your usual self and… … you felt so good or so hyper that other people thought you were not your normal self or you were so hyper that you got into trouble? … you were so irritable that you shouted at people or started fights or arguments? … you felt much more self-confident than usual? … you got much less sleep than usual and found you didn’t really miss it? … you were much more talkative or spoke much faster than usual? … thoughts raced through your head or you couldn’t slow your mind down? Hirschfeld et al. Am J Psychiatry. 2000;157:1873-1875. Mood Disorder Questionnaire (cont’d) … you were so easily distracted by things around you that you had trouble concentrating or staying on track? … you had much more energy than usual? … you were much more active or did many more things than usual? … you were much more social or outgoing than usual; for example, you telephoned friends in the middle of the night? … you were much more interested in sex than usual? … you did things that were unusual for you or that other people might have thought were excessive, foolish, or risky? … spending money got you or your family into trouble? Hirschfeld et al. Am J Psychiatry. 2000;157:1873-1875. Depression Adolescents 30% BPAD switch Irritability Adults 10% switch Sadness Long-term Frequency of Depressive Symptoms (Percent of Follow-up Weeks) Patients with bipolar I disorder experienced mood symptoms nearly half of the time during a 12.8-year follow-up period. Depressive symptoms were predominant • Over the long term, patients with bipolar I disorder spent nearly half of their time symptomatically ill • Depression accounted for 31.9% of the time • Patients experienced manic symptoms 9.3% of the time • Depression (but not mania) predicted greater future illness burden Judd et al. Arch Gen Psychiatry. 2002;59:530-537. Age of Onset (Pooled Data N=1,304) 500 400 300 # of Pts 200 100 0 Under 10 10-19 20-29 30-39 40-49 50-59 60-69 70 and Over Age of Onset Goodwin F, Jamison K. Manic Depression. New York: Oxford University Press; 1990. Predictors of BPAD Outcome Acute onset Hypersomnic retarded depression Psychosis Postpartum onset Family history Antidepressant Hypersomnia Treatment for Depression Non-Medical Txment of Depression Cognitive Behavioral Therapy (CBT) Dialectical behavior therapy (DBT) Mindfulness NEUROTRANSMITTER EFFECTS OF ANTIDEPRESSANTS NE Bupropion SR 5-HT DA SSRIs Venlafaxine Nefazodone Mirtazapine Desipramine Richelson. J Clin Psychiatry. 1994 The role of BDNF and its receptors in depression and antidepressant drug action: Reactivation of developmental plasticity Recent evidence suggests that neuronal plasticity plays an important role in the recovery from depression. Antidepressant drugs and electroconvulsive shock treatment increase the expression of several molecules, which are associated with neuronal plasticity, in particular the neurotrophin BDNF and its receptor TrkB. Furthermore, these treatments increase neurogenesis and synaptic numbers in several brain areas. Conversely, depression, at least in its severe form, is associated with reduced volumes of the hippocampus and prefrontal cortex and in at least some cases these neurodegenerative signs can be attenuated by successful treatment. Such observations suggest a central role for neuronal plasticity in depression and the antidepressant effect, and also implicate BDNF signaling as a mediator of this plasticity. The antidepressant fluoxetine can reactivate developmental-like neuronal plasticity in the adult visual cortex, which, under appropriate environmental guidance, leads to the rewiring of a developmentally dysfunctional neural network. These observations suggest that the simple form of the neurotrophic hypothesis of depression, namely, that deficient levels of neurotrophic support underlies mood disorders and increases in these neurotrophic factors to normal levels brings about mood recovery, may not sufficiently explain the complex process of recovery from depression. This review discusses recent data on the role of BDNF and its receptors in depression and the antidepressant response and suggests a model whereby the effects of antidepressant treatments could be explained by a reactivation of activity-dependent and BDNF-mediated cortical plasticity, which in turn leads to the adjustment of neuronal networks to better adapt to environmental challenges. © 2010 Wiley Periodicals, Inc. Develop Neurobiol 2010 Somatic Depression Treatment Bupropion Serotonin (re)-uptake inhibitors TCA’s (Tricyclic Antidepressant) Others: Nefazodone, Trazadone, Mirtazapine, Venlafaxine, duloxetine MAOI’s (including Selegiline (Emsam patch)) ECT Trancranial Magnetic Stimulation (TMS) Newer Antidepressants Vilazodone (Viibryd): diarrhea, nausea or vomiting, and trouble sleeping, increases serotonin. Vortioxetine (Brintellix): nausea, constipation, and vomiting, increases serotonin Levomilnacacipran (Fetzima): nausea or vomiting, constipation, sweating, increased heart rate, erectile dysfunction, and palpitations, increases serotonin and norepinephrine. Things to consider with meds Comorbidities: anxiety, subst. abuse, Compliance Formulary (preferred drug list) Medical legal Indication (“Off Label?”) Side Effects Treatment: Lamotrigine (Lamictal) Positives: Once a day dosing possible No Blood tests Few complaints of SE’s Negatives Long time to get up to good dose Rash ? Neuroleptics (antipsychotics) Mood Disorders (primarily BD) Schizophrenia/Schizoaffective Some Sxs of PTSD Clozapine WBC monitoring Constipation Dizziness Sedation Miracle Aripiprazole (Abilify) Wgt neutral?, EPS, Nonsedating, Agitation FDA approved ABILIFY® (aripiprazole) for the acute treatment of manic and mixed episodes, maintenance treatment of manic or mixed episodes, and as add-on treatment to lithium or valproate, associated with Bipolar I Disorder, with or without psychotic features, and schizophrenia in pediatric patients (10 to 17 years old). Refractoy Depression Treatment: Risperidone (Risperdal) Positives: No blood tests Once a day dosing Fast Shotgun FDA approved Risperdal (risperidone) for the treatment of schizophrenia in adolescents, ages 13 to 17, and for the shortterm treatment of manic or mixed episodes of bipolar I disorder in children and adolescents ages 10 to 17. Negatives: Prolactin Some reports of mania induction Weight gain Sedation NMS Tardive dyskinesia Diabetes risk Treatment: Olanzapine (Zyprexa) Positives: No blood tests Once a day dosing Data FDA indication Fast Shotgun Negatives: Sedation Weight gain Diabetes risk Ziprasidone (Geodon) Wgt neutral Sedating vs activating Efficacy? Quetiapine (Seroquel) Midrange sedation Midrange wgt gain Diabetes risk Refractory Depression Bipolar Depression Treatment: Lithium Positives: Low suicide rates FDA approved 12yrs and older Long history of use Once a day dosing Cheap Negatives: Narrow therapeutic window Fluid balance issues Monitoring (thyroid & kidney) Acne Weight The 3 Newest Lurasidone (Latuda): (Bipolar Depression)Once a day, with food, sedation and EPS Asenapine (Saphris): Once a day, disolves in mouthsome find unpleasant taste Iloperidone (Fanapt) Twice a day Buproprion For Prevention of Depressive sx’s SADS Hospice family members Combined therapy: symptoms/ cooccurring conditions ADHD: stimulants, bupropion, ?modafinil Anxiety: (OCD too) gabapentine, tiagabine, SSRI, TCA Depression: ECT, additional mood stabilizer (lamotrigine), antidepressant if we must Fatigue: modafinil, stimulants Insomnia: benzodiazepines, neuroleptics, mirtazepine, trazadone Mania: mood stabilizer, neuroleptic The Good News Neurotrophic Effects of Mood Stabilizers? MRI studies “…revealed that chronic lithium significantly increases total grey mattervolume in the human brain of patients with manicdepressive illness. Neuroprotective? “…lithium and valproate have recently been demonstrated to robustly increase the expression of the cytoprotective protein bcl-2 in the central nervous system.” Husseini et. al. From a Mouth Swab “Your doctor may use cytochrome P450 tests (CYP450 tests) to help determine how your body processes (metabolizes) a drug. Our bodies contain numerous P450 enzymes to process medications. Because of inherited (genetic) traits which cause variations in these enzymes, medications affect each person differently.” Genetic Testing Future Trends Summary Earlier Identification and Aggressive Txmnt Increase focus on primary and especially secondary Prevention Neurotransmitter and enzyme specific treatment. More delineation of “Normal” behavior and it’s relationship to our genes. More Exploration of Combined Therapy Remission not just response